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  1 / 209 MEDLINE  
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[PMID]:27993290
[Au] Autor:Horikiri T; Hara H; Saito N; Araya J; Takasaka N; Utsumi H; Yanagisawa H; Hashimoto M; Yoshii Y; Wakui H; Minagawa S; Ishikawa T; Shimizu K; Numata T; Arihiro S; Kaneko Y; Nakayama K; Matsuura T; Matsuura M; Fujiwara M; Okayasu I; Ito S; Kuwano K
[Ad] Endereço:Division of Respiratory Diseases, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.
[Ti] Título:Increased levels of prostaglandin E-major urinary metabolite (PGE-MUM) in chronic fibrosing interstitial pneumonia.
[So] Source:Respir Med;122:43-50, 2017 Jan.
[Is] ISSN:1532-3064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dysregulation of the prostaglandin E2 (PGE2) signaling pathway has been implicated in interstitial pneumonia (IP) pathogenesis. Due to the unstable nature of PGE2, available detection methods may not precisely reflect PGE2 levels. We explored the clinical usefulness of measuring stable prostaglandin E-major urinary metabolite (PGE-MUM) with respect to pathogenesis and extent of chronic fibrosing IP (CFIP), including idiopathic pulmonary fibrosis (IPF), as PGE-MUM is reflective of systemic PGE2 production. METHODS: PGE-MUM was measured by radioimmunoassay in controls (n = 124) and patients with lung diseases (bronchial asthma (BA): n = 78, chronic obstructive pulmonary disease (COPD): n = 33, CFIP: n = 44). Extent of lung fibrosis was assessed by fibrosing score (FS) of computed tomography (CT) (FS1-4). Immunohistochemical evaluation of COX-2 was performed to find PGE2 producing cells in IPF. Human bronchial epithelial cells (HBEC) and lung fibroblasts (LFB) were used in in vitro experiments. RESULTS: Compared to control, PGE-MUM levels were significantly elevated in CFIP. PGE-MUM levels were positively correlated with FS, and inversely correlated with %DLCO in IP (FS 1-3). COX-2 was highly expressed in metaplastic epithelial cells in IPF, but lower expression of EP2 receptor was demonstrated in LFB derived from IPF. TGF-ß induced COX-2 expression in HBEC. CONCLUSIONS: PGE-MUM, elevated in CFIP, is a promising biomarker reflecting disease activity. Metaplastic epithelial cells can be a source of elevated PGE-MUM in IPF.
[Mh] Termos MeSH primário: Fibrose Pulmonar Idiopática/metabolismo
Doenças Pulmonares Intersticiais/metabolismo
Pulmão/metabolismo
Ácidos Prostanoicos/análise
Urina/química
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/metabolismo
Ciclo-Oxigenase 2/metabolismo
Células Epiteliais/metabolismo
Feminino
Fibroblastos/metabolismo
Seres Humanos
Fibrose Pulmonar Idiopática/diagnóstico por imagem
Fibrose Pulmonar Idiopática/patologia
Japão/epidemiologia
Pulmão/patologia
Doenças Pulmonares Intersticiais/diagnóstico por imagem
Doenças Pulmonares Intersticiais/patologia
Masculino
Meia-Idade
Prostaglandinas/metabolismo
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Prostaglandins); 0 (Prostanoic Acids); 0 (Transforming Growth Factor beta); 24769-56-0 (11 alpha-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostanoic acid); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


  2 / 209 MEDLINE  
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[PMID]:27352806
[Au] Autor:Tsikas D
[Ad] Endereço:Centre of Pharmacology and Toxicology, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625, 30623 Hannover, Germany. Electronic address: tsikas.dimitros@mh-hannover.de.
[Ti] Título:GC-ECNICI-MS/MS of eicosanoids as pentafluorobenzyl-trimethylsilyl (TMS) derivatives: Evidence of CAD-induced intramolecular TMS ether-to-ester rearrangement using carboxy- O-labelled eicosanoids and possible implications in quantitative analysis.
[So] Source:J Chromatogr B Analyt Technol Biomed Life Sci;1047:185-196, 2017 Mar 15.
[Is] ISSN:1873-376X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:GC-MS and GC-MS/MS of pentafluorobenzyl (PFB) ester trimethylsilyl (TMS) ether (PFB-TMS) derivatives of hydroxylated long-chain fatty acids including arachidonic acid metabolites, the eicosanoids, in the electron-capture negative-ion chemical ionization (ECNICI) mode are the most sensitive and accurate approaches to quantify carboxyl groups-containing compounds in complex biological fluids such as plasma and urine. Under ECNICI conditions, PFB-TMS derivatives of eicosanoids ionize to form very few ions, with the carboxylates [M-PFB] being typically the most intense. Less intense ions may be additionally formed by consecutive neutral loss (NL) of trimethylsilanol (TMSOH, 90Da) groups ([M-PFB-(TMSOH) ] ). By using [1,1- O ]- and [1,ω- O ]-eicosanoids, we studied ion processes following collisionally activated dissociation (CAD) of the precursor ions [M-PFB] . We found that CAD resulted in formation of product ions due to NL of a TMS OH (92Da) group in monocarboxylic and of a PFB OH (200Da) group in dicarboxylic eicosanoids. TMS OH NL implies an intra-molecular transfer of the TMS group from hydroxyl groups to their carboxylate anions [M-PFB] . From a mechanistic point of view, this rearrangement may explain formation of unique product ions in GC-MS/MS of eicosanoids under ECNICI conditions. From the quantitative point of view, quantification by GC-MS/MS of product ions due to [M-PFB-(TMSOH) ] and [M-PFB-TMS OH-(TMSOH) ] would reveal incorrect data, if [1,1- O ]-eicosanoids are used as internal standards and if no correction for the O-loss is performed. In O-labelled dicarboxylic eicosanoids, such as the major urinary metabolite (MUM) of E prostaglandins, i.e., [1,ω- O ]-PGE-MUM), no TMS ester/TMS ether rearrangement was observed. Yet, O-loss occurred upon CAD of [M-PFB] due to NL of PFB OH (200Da). In both cases the extent of O-loss needs to be determined and considered for accurate quantification of monocarboxylic acids such as 8-isoprostaglandin F (8-iso-PGF ) and dicarboxylic eicosanoids such as PGE-MUM.
[Mh] Termos MeSH primário: Eicosanoides/análise
Fluorbenzenos/química
Cromatografia Gasosa-Espectrometria de Massas/métodos
Compostos de Trimetilsilil/química
[Mh] Termos MeSH secundário: Ésteres/química
Seres Humanos
Isótopos de Oxigênio/análise
Isótopos de Oxigênio/urina
Ácidos Prostanoicos/análise
Ácidos Prostanoicos/urina
Espectrometria de Massas em Tandem/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Eicosanoids); 0 (Esters); 0 (Fluorobenzenes); 0 (Oxygen Isotopes); 0 (Prostanoic Acids); 0 (Trimethylsilyl Compounds); 24769-56-0 (11 alpha-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostanoic acid)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170322
[Lr] Data última revisão:
170322
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160630
[St] Status:MEDLINE


  3 / 209 MEDLINE  
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[PMID]:26788915
[Au] Autor:Arai Y; Matsuura T; Matsuura M; Fujiwara M; Okayasu I; Ito S; Arihiro S
[Ad] Endereço:Division of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
[Ti] Título:Prostaglandin E-Major Urinary Metabolite as a Biomarker for Inflammation in Ulcerative Colitis: Prostaglandins Revisited.
[So] Source:Digestion;93(1):32-9, 2016.
[Is] ISSN:1421-9867
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:With the development of new therapeutic approaches, the ultimate goal of ulcerative colitis (UC) treatment is not only clinical remission but also mucosal healing. Successful mucosal healing has been associated with a dramatic risk reduction in UC recurrence and colitis-associated cancer development, which are the most critical complications of UC. However, invasive tests such as colonoscopy and biopsy are required to evaluate mucosal healing. Therefore, frequent examinations are unsuitable for UC patients. Mucosal inflammation of the colon and prostaglandin E2 production are assumed to be correlated; therefore, we considered that prostaglandin E-major urinary metabolite (PGE-MUM; 7-hydroxy-5,11-diketotetranor-prosta-1,16-dioic acid) may be a surrogate biomarker of UC activity. In this review, we propose that PGE-MUM levels reflect the colonoscopic and histological appearance of UC, suggesting that it is a more sensitive biomarker than those previously utilized for UC-related mucosal inflammation. According to the 'organ-specific chronic inflammation-carcinoma sequence' theory, by measuring PGE-MUM periodically, it would be possible to control inflammation, with subsequent prevention of UC recurrence and colitis-associated cancer development. The measurement of urine samples for PGE-MUM - a simple, noninvasive method - can reduce the patient burden as well as medical costs, suggesting its potential for application in routine practice.
[Mh] Termos MeSH primário: Colite Ulcerativa/urina
Ácidos Prostanoicos/urina
[Mh] Termos MeSH secundário: Biomarcadores/urina
Biópsia
Carcinogênese/imunologia
Carcinoma/imunologia
Colite Ulcerativa/imunologia
Colite Ulcerativa/patologia
Neoplasias do Colo/imunologia
Colonoscopia
Dinoprostona/imunologia
Enterite/imunologia
Enterite/patologia
Seres Humanos
Mucosa Intestinal/imunologia
Mucosa Intestinal/patologia
Ácidos Prostanoicos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Prostanoic Acids); 24769-56-0 (11 alpha-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostanoic acid); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160121
[St] Status:MEDLINE
[do] DOI:10.1159/000441665


  4 / 209 MEDLINE  
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[PMID]:26355965
[Au] Autor:Lukasik B; Perlikowska W; Zurawinski R; Mikolajczyk M
[Ad] Endereço:Department of Heteroorganic Chemistry, Center of Molecular and Macromolecular Studies, Polish Academy of Sciences , Sienkiewicza 112, 90-363 Lódz, Poland.
[Ti] Título:Synthesis of Enantiomerically Pure Stereomers of Rosaprostol.
[So] Source:J Org Chem;80(19):9798-802, 2015 Oct 02.
[Is] ISSN:1520-6904
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enantiopure stereomers of rosaprostol 1, an antiulcer drug, were synthesized from diastereomeric building blocks (-)-5a and (+)-5b. Conversion of (-)-5a into rosaprostol stereomer (-)-(1S,2R,5R)-1a was accomplished in nine steps in 18% overall yield. In this sequence, fully diastereoselective hydrogeneration of the endocyclic carbon double bond in the cyclopentenone ring was key, generating a new stereogenic center (C-2 in 1a). C-5 epimeric rosaprostol (-)-(1S,2R,5S)-1b was obtained from (-)-1a in 72% yield by a two-reaction sequence involving methylation and one-pot Mitsunobu esterification-hydrolysis.
[Mh] Termos MeSH primário: Ácidos Prostanoicos/síntese química
[Mh] Termos MeSH secundário: Esterificação
Hidrólise
Estrutura Molecular
Ácidos Prostanoicos/química
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Prostanoic Acids); W4459A2P0J (rosaprostol)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151002
[Lr] Data última revisão:
151002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150911
[St] Status:MEDLINE
[do] DOI:10.1021/acs.joc.5b01749


  5 / 209 MEDLINE  
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[PMID]:21606476
[Au] Autor:Buckley J; Birrell MA; Maher SA; Nials AT; Clarke DL; Belvisi MG
[Ad] Endereço:Respiratory Pharmacology, Pharmacology and Toxicology Section, Imperial College London, Faculty of Medicine, National Heart and Lung Institute, Sir Alexander Fleming Building, London SW7 2AZ, UK.
[Ti] Título:EP4 receptor as a new target for bronchodilator therapy.
[So] Source:Thorax;66(12):1029-35, 2011 Dec.
[Is] ISSN:1468-3296
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Asthma and chronic obstructive pulmonary disease are airway inflammatory diseases characterised by airflow obstruction. Currently approved bronchodilators such as long-acting ß(2) adrenoceptor agonists are the mainstay treatments but often fail to relieve symptoms of chronic obstructive pulmonary disease and severe asthma and safety concerns have been raised over long-term use. The aim of the study was to identify the receptor involved in prostaglandin E(2) (PGE(2))-induced relaxation in guinea pig, murine, monkey, rat and human airways in vitro. METHODS: Using an extensive range of pharmacological tools, the relaxant potential of PGE(2) and selective agonists for the EP(1-4) receptors in the presence and absence of selective antagonists in guinea pig, murine, monkey, rat and human isolated airways was investigated. RESULTS: In agreement with previous studies, it was found that the EP(2) receptor mediates PGE(2)-induced relaxation of guinea pig, murine and monkey trachea and that the EP(4) receptor mediates PGE(2)-induced relaxation of the rat trachea. These data have been confirmed in murine airways from EP(2) receptor-deficient mice (Ptger2). In contrast to previous publications, a role for the EP(4) receptor in relaxant responses in human airways in vitro was found. Relaxant activity of AH13205 (EP(2) agonist) was also demonstrated in guinea pig but not human airway tissue, which may explain its failure in clinical studies. CONCLUSION: Identification of the receptor mediating PGE(2)-induced relaxation represents a key step in developing a novel bronchodilator therapy. These data explain the lack of bronchodilator activity observed with selective EP(2) receptor agonists in clinical studies.
[Mh] Termos MeSH primário: Asma/tratamento farmacológico
Broncodilatadores/farmacologia
Dinoprostona/farmacologia
Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico
Receptores de Prostaglandina E/agonistas
Traqueia/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alprostadil/análogos & derivados
Alprostadil/farmacologia
Animais
Asma/fisiopatologia
Dinoprostona/análogos & derivados
Cobaias
Seres Humanos
Hidrazinas/farmacologia
Macaca fascicularis
Éteres Metílicos/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Naftalenos/farmacologia
Fenilbutiratos/farmacologia
Ácidos Prostanoicos/farmacologia
Doença Pulmonar Obstrutiva Crônica/fisiopatologia
Ratos
Ratos Sprague-Dawley
Receptores de Prostaglandina E/fisiologia
Análise de Regressão
Especificidade da Espécie
Traqueia/fisiologia
Xantonas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-(4-cyano-2-(2-(4-fluoronaphthalen-1-yl)propionylamino)phenyl)butyric acid); 0 (9-deoxy-9-chloro-15-deoxy-16-hydroxy-17,17-trimethylene-19,20-didehydroprostaglandin E2); 0 (Bronchodilator Agents); 0 (Hydrazines); 0 (Methyl Ethers); 0 (Naphthalenes); 0 (ONO AE 248); 0 (ONO-AE1-329); 0 (ONO-DI-004); 0 (Phenylbutyrates); 0 (Prostanoic Acids); 0 (Receptors, Prostaglandin E); 0 (Xanthones); 148436-63-9 (AH 13205); 33458-93-4 (6-isopropoxy-9-oxoxanthene-2-carboxylic acid); 98299-61-7 (SQ 29548); F5TD010360 (Alprostadil); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1201
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110525
[St] Status:MEDLINE
[do] DOI:10.1136/thx.2010.158568


  6 / 209 MEDLINE  
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[PMID]:19476545
[Au] Autor:Takahashi K; Niidome T; Akaike A; Kihara T; Sugimoto H
[Ad] Endereço:Department of Neuroscience for Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
[Ti] Título:Amyloid precursor protein promotes endoplasmic reticulum stress-induced cell death via C/EBP homologous protein-mediated pathway.
[So] Source:J Neurochem;109(5):1324-37, 2009 Jun.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) is known to activate the ER, which is termed ER stress. Here, we demonstrated that amyloid precursor protein (APP) is a novel mediator of ER stress-induced apoptosis through the C/EBP homologous protein (CHOP) pathway. Expression of APP mRNA was elevated by tunicamycin- or dithiothreitol-induced ER stress. The levels of C83 and APP intracellular domain (AICD) fragments, which are cleaved from APP, were significantly increased under ER stress, although the protein level of full-length APP was decreased. Cellular viability was reduced in APP-over-expressing cells, which was attenuated by treatment with a gamma-secretase inhibitor, N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT). Cellular viability was also reduced in AICD-FLAG-over-expressing cells. The mRNA and protein levels of CHOP, an ER stress-responsive gene, were remarkably increased by APP over-expression, which was attenuated by treatment with DAPT. CHOP mRNA induction was also found in AICD-FLAG-over-expressing cells. Cell death and CHOP up-regulation by ER stress were attenuated by APP knockdown. Data obtained with a luciferase assay and chromatin immunoprecipitation assay indicated that AICD associates with the promoter region of the CHOP gene. In conclusion, ER stress-induced APP undergoes alpha- and gamma-secretase cleavage and subsequently induces CHOP-mediated cell death.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Retículo Endoplasmático/metabolismo
Transdução de Sinais/fisiologia
Estresse Fisiológico/efeitos dos fármacos
Fator de Transcrição CHOP/metabolismo
[Mh] Termos MeSH secundário: Peptídeos beta-Amiloides/metabolismo
Precursor de Proteína beta-Amiloide/genética
Morte Celular/efeitos dos fármacos
Linhagem Celular/ultraestrutura
Imunoprecipitação da Cromatina/métodos
Dipeptídeos/farmacologia
Ditiotreitol/farmacologia
Retículo Endoplasmático/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Seres Humanos
L-Lactato Desidrogenase/metabolismo
Neuroblastoma
Ácidos Prostanoicos/metabolismo
Estrutura Terciária de Proteína/fisiologia
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/farmacologia
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Transfecção
Tunicamicina/farmacologia
Tirosina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (DDIT3 protein, human); 0 (Dipeptides); 0 (Enzyme Inhibitors); 0 (N-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester); 0 (Prostanoic Acids); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 11089-65-9 (Tunicamycin); 147336-12-7 (Transcription Factor CHOP); 42HK56048U (Tyrosine); EC 1.1.1.27 (L-Lactate Dehydrogenase); T8ID5YZU6Y (Dithiothreitol); W4459A2P0J (rosaprostol)
[Em] Mês de entrada:0906
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090530
[St] Status:MEDLINE
[do] DOI:10.1111/j.1471-4159.2009.06067.x


  7 / 209 MEDLINE  
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[PMID]:18534756
[Au] Autor:Tanahashi H; Yoshioka K
[Ad] Endereço:Division of Molecular Cell Signaling, Cancer Research Institute, Kanazawa University, 13-1 Takaramachi, Kanazawa, Ishikawa 920-0934, Japan. tanahashi_h@ybb.ne.jp
[Ti] Título:RNA interference silencing of DRAL affects processing of amyloid precursor protein.
[So] Source:Neurosci Lett;439(3):293-7, 2008 Jul 18.
[Is] ISSN:0304-3940
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In a previous study, we reported that Alzheimer's disease-associated presenilin-2 interacts with a LIM-domain protein, namely, DRAL/FHL2/SLIM3. In this study, we investigated whether DRAL modifies the metabolism of the amyloid precursor protein (APP). We used small interfering RNA (siRNA) to knockdown DRAL in COS7 and HEK293 cells that stably overexpress APP695. We found that the knockdown was accompanied by a decrease in the amount of secreted alpha-secretase-cleaved APP and the membrane-bound C-terminal fragment C83 and an increase in the amount of secreted beta-amyloid peptide (Abeta) from the cells. We also found that in addition to a disintegrin and metalloprotease (ADAM)-17, DRAL binds to ADAM-10. Thus, DRAL may be involved in the processing of APP through the alpha-secretase pathway.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Proteínas de Homeodomínio/metabolismo
Proteínas Musculares/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Proteínas ADAM/metabolismo
Proteína ADAM10
Proteína ADAM17
Secretases da Proteína Precursora do Amiloide/metabolismo
Animais
Linhagem Celular Transformada
Cercopithecus aethiops
Cricetinae
Seres Humanos
Proteínas com Homeodomínio LIM
Proteínas de Membrana/metabolismo
Ésteres de Forbol/farmacologia
Ácidos Prostanoicos/metabolismo
RNA Interferente Pequeno/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (FHL2 protein, human); 0 (Homeodomain Proteins); 0 (LIM-Homeodomain Proteins); 0 (Membrane Proteins); 0 (Muscle Proteins); 0 (Phorbol Esters); 0 (Prostanoic Acids); 0 (RNA, Small Interfering); 0 (Transcription Factors); 20839-06-9 (phorbol-12-myristate); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human); W4459A2P0J (rosaprostol)
[Em] Mês de entrada:0809
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080607
[St] Status:MEDLINE
[do] DOI:10.1016/j.neulet.2008.05.039


  8 / 209 MEDLINE  
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[PMID]:17993463
[Au] Autor:Song WL; Wang M; Ricciotti E; Fries S; Yu Y; Grosser T; Reilly M; Lawson JA; FitzGerald GA
[Ad] Endereço:Institute for Translational Medicine and Therapeutics, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
[Ti] Título:Tetranor PGDM, an abundant urinary metabolite reflects biosynthesis of prostaglandin D2 in mice and humans.
[So] Source:J Biol Chem;283(2):1179-88, 2008 Jan 11.
[Is] ISSN:0021-9258
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostaglandin D(2) (PGD(2)) is a cyclooxygenase (COX) product of arachidonic acid that activates D prostanoid receptors to modulate vascular, platelet, and leukocyte function in vitro. However, little is known about its enzymatic origin or its formation in vivo in cardiovascular or inflammatory disease. 11,15-dioxo-9alpha-hydroxy-2,3,4,5-tetranorprostan-1,20-dioic acid (tetranor PGDM) was identified by mass spectrometry as a metabolite of infused PGD(2) that is detectable in mouse and human urine. Using liquid chromatography-tandem mass spectrometry, tetranor PGDM was much more abundant than the PGD(2) metabolites, 11beta-PGF(2alpha) and 2,3-dinor-11beta-PGF(2alpha), in human urine and was the only endogenous metabolite detectable in mouse urine. Infusion of PGD(2) dose dependently increased urinary tetranor PGDM > 2,3-dinor-11beta-PGF(2alpha) > 11beta-PGF(2alpha) in mice. Deletion of either lipocalin-type or hemopoietic PGD synthase enzymes decreased urinary tetranor PGDM. Deletion or knockdown of COX-1, but not deletion of COX-2, decreased urinary tetranor PGDM in mice. Correspondingly, both PGDM and 2,3-dinor-11beta-PGF(2alpha) were suppressed by inhibition of COX-1 and COX-2, but not by selective inhibition of COX-2 in humans. PGD(2) has been implicated in both the development and resolution of inflammation. Administration of bacterial lipopolysaccharide coordinately elevated tetranor PGDM and 2,3-dinor-11beta-PGF(2alpha) in volunteers, coincident with a pyrexial and systemic inflammatory response, but both metabolites fell during the resolution phase. Niacin increased tetranor PGDM and 2,3-dinor-11beta-PGF(2alpha) in humans coincident with facial flushing. Tetranor PGDM is an abundant metabolite in urine that reflects modulated biosynthesis of PGD(2) in humans and mice.
[Mh] Termos MeSH primário: Prostaglandina D2/análogos & derivados
Prostaglandina D2/biossíntese
Ácidos Prostanoicos/urina
[Mh] Termos MeSH secundário: Animais
Cromatografia Líquida de Alta Pressão
Inibidores de Ciclo-Oxigenase/farmacologia
Dimerização
Seres Humanos
Oxirredutases Intramoleculares/deficiência
Oxirredutases Intramoleculares/genética
Oxirredutases Intramoleculares/metabolismo
Lactonas/farmacologia
Lipocalinas/genética
Lipocalinas/metabolismo
Masculino
Espectrometria de Massas
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Prostaglandina D2/urina
Sulfonas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (11,15-dioxo-9-hydroxy-2,3,4,5-tetranorprostan-1,20-dioic acid); 0 (Cyclooxygenase Inhibitors); 0 (Lactones); 0 (Lipocalins); 0 (Prostanoic Acids); 0 (Sulfones); 0QTW8Z7MCR (rofecoxib); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.99.2 (prostaglandin R2 D-isomerase); RXY07S6CZ2 (Prostaglandin D2)
[Em] Mês de entrada:0803
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:071113
[St] Status:MEDLINE


  9 / 209 MEDLINE  
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[PMID]:16783171
[Au] Autor:Auerbach ID; Vinters HV
[Ad] Endereço:Department of Pathology and Laboratory Medicine (Neuropathology), the Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
[Ti] Título:Effects of anoxia and hypoxia on amyloid precursor protein processing in cerebral microvascular smooth muscle cells.
[So] Source:J Neuropathol Exp Neurol;65(6):610-20, 2006 Jun.
[Is] ISSN:0022-3069
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cerebral amyloid angiopathy (CAA) is characterized by the degeneration of cerebral microvascular smooth muscle cells (MV-SMC) and the replacement of normal vessel wall components by beta-amyloid (Abeta) protein. Little is known regarding the mechanisms of SMC degeneration in CAA. The effects of anoxia on the metabolism of the amyloid precursor protein (APP) were studied to investigate the MV-SMC response to anoxic stress and its possible role in the pathogenesis of CAA. MV-SMC exposed to chronic anoxia (24-48 hours) showed a decrease in expression of the 2 putative alpha-secretase enzymes, mature TACE (TNFalpha-converting enzyme) and ADAM10 (a disintegrin and metalloprotease). A concomitant decrease in the alpha-secretase cleavage products sAPPalpha and C83 was observed. Investigation of mRNA expression showed an increase in TACE and a sharp decrease in ADAM10 at 24 hours. Exposing MV-SMC to hypoxia (1% O2) revealed a different pattern of expression with no significant change in TACE protein, but an increase in TACE mRNA occurring at a later time point (48 hours). There was no change in ADAM10 mRNA expression, but a reduction in mature ADAM10 with a parallel increase in immature ADAM10 protein. These results demonstrate a requirement for oxygen in the regulation of the alpha-secretase pathway during APP metabolism.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Hipóxia/metabolismo
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Proteínas ADAM/metabolismo
Proteína ADAM10
Proteína ADAM17
Secretases da Proteína Precursora do Amiloide
Western Blotting/métodos
Células Cultivadas
Córtex Cerebral/citologia
Regulação da Expressão Gênica/fisiologia
Seres Humanos
Hipóxia/patologia
Imunoprecipitação
Proteínas de Membrana/metabolismo
Ácidos Prostanoicos/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (APLP1 protein, human); 0 (Amyloid beta-Protein Precursor); 0 (Membrane Proteins); 0 (Prostanoic Acids); 0 (RNA, Messenger); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human); W4459A2P0J (rosaprostol)
[Em] Mês de entrada:0608
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060620
[St] Status:MEDLINE


  10 / 209 MEDLINE  
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[PMID]:16464089
[Au] Autor:Ohmiya H; Yorimitsu H; Oshima K
[Ad] Endereço:Department of Material Chemistry, Graduate School of Engineering, Kyoto University, Kyoto-daigaku Katsura, Nishikyo-ku, Kyoto 615-8510, Japan.
[Ti] Título:Cobalt(diamine)-catalyzed cross-coupling reaction of alkyl halides with arylmagnesium reagents: stereoselective constructions of arylated asymmetric carbons and application to total synthesis of AH13205.
[So] Source:J Am Chem Soc;128(6):1886-9, 2006 Feb 15.
[Is] ISSN:0002-7863
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A cobalt-diamine complex catalyzes the cross-coupling reactions of primary and secondary alkyl halides with aryl Grignard reagents. It is confirmed that oxidative addition of alkyl halide to cobalt proceeds via a radical process. Optically pure Ueno-Stork halo acetals undergo diastereoselective cross-coupling reactions, the products of which are transformed into optically active THF derivatives. A sequential radical cyclization/arylation reaction under cobalt catalysis provides extremely short access to a synthetic prostaglandin AH13205.
[Mh] Termos MeSH primário: Cobalto/química
Hidrocarbonetos Halogenados/química
Magnésio/química
Ácidos Prostanoicos/síntese química
[Mh] Termos MeSH secundário: Catálise
Ciclização
Compostos Organometálicos/química
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydrocarbons, Halogenated); 0 (Organometallic Compounds); 0 (Prostanoic Acids); 148436-63-9 (AH 13205); 3G0H8C9362 (Cobalt); I38ZP9992A (Magnesium)
[Em] Mês de entrada:0604
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060209
[St] Status:MEDLINE



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